An important new research article for dog (and cat) behaviorists who deal with fear, anxiety, and behavior modification was published in the premier journal Science during Christmas week of last year (2011). Let me set the stage, and then describe the findings.

Fear and anxiety is one of the most common sources of aggressive, and other, behavior issues (not dominance and pack leadership, as some trainers suggest). This is also a widespread issue in the human population: fear, phobia, anxiety, and serious conditions such as post-traumatic stress disorder can be debilitating. All of these fear or anxiety related disorders stem from a fundamental problem, a disregulation, of the neurotransmitters in the brain. This may be caused by genetic or developmental issues: anxiety, obsessive-compulsive disorder and other related conditions have been shown to have possible genetic causes. But more frequently, anxiety is caused by an exposure to a fearful, scary, stressful, or (mentally or physically) traumatic situation, or more likely, multiple exposures.

In this case, the neurons in the brain adjust the levels of neurotransmitter chemicals (the communication bonds of the nervous system); if the stressor is repeated, or occurs at a very sensitive time in develop of the brain, this adjustment can become permanent, producing not a passing fear or anxiety response, but an ongoing, hypersensitive response. In dogs who are traumatized by children at a critical time for brain development, or exposed to repeated punishment, or who receive inappropriate or too little socialization at the right age, this chronic change in the brain can result in fear, and is frequently manifested as aggression, even in inappropriate situations. That’s where veterinarians and behavior specialists often get involved.

We know that a process called counterconditioning, where positive rewards are consistently and repeatedly linked to sub-threshold exposures to anxiety-producing stimuli can, if done correctly, significantly reduce the fear response. But we also know that in some cases, it does not work, and in some cases (many cases!), we see a rebound effect, where the fear response reappears after counterconditioning ends.

We also have several families of medications that specifically target these neurotransmitters, altering levels of these chemicals in the brain and thus lowering anxiety in general, and in response to the scary stimuli, whatever it might be.

Finally, we have known clinically for some time that pairing the use of counterconditioning, or what might be called ‘extinction training’ (repeated exposure to the scary stimuli without anything scary happening, or in our case, even with something good happening) with the use of one of these modern anti-anxiety medications has been extremely effective. But we have not known why!

The research published in this paper gives us the first experimental confirmation that this effect is real, and confirmation of a hypothesis about why this synergistic interaction between training and medication occurs. In the research described in this paper, biologists induced an anxiety response in mice, and then extinguished that response in the presence or absence of fluoxetine (commonly known as Prozac). They examined the rate of extinction of the anxiety response, and then later tested the mice for a rebound or recovery of the anxiety response. Finally, they examined the neuronal cells in the brain of these mice to see what had actually changed.

The results? Fascinating! First, they found exactly the effect that many of us have seen clinically: extinction of response occurred more quickly in the presence of fluoxetine, while the use of either extinction training or fluoxetine separately was less effective. The rebound effect was also documented, and was significantly less intense when both extinction and fluoxetine were used together. In fact, when the two were used together, the rebound effect did not occur.

So why does this happen? It turns out that the fluoxetine shifts the maturation clock of the neurons backwards to an earlier, more impressionable state. It is like the brain becomes plastic again; open to input and shaping by the environment. It’s a Reset button! Treatment with fluoxetine makes the neurons more amenable to learning and shaping, to responding to the information that the stimulus that the mice had learned was scary is no longer scary. Now the stimulus is either not scary, or in the case of our counterconditioning, even perceived as positive, and the neurons are in a state in which they can take in or use this information to form (more desirable) permanent connections. Thus, no rebound effect: in the case of positive training without medication, at least in some cases, we can only bend the neurons to where we want them, and when we stop “bending” them, they return to their previous state: fearful.

So from a practical point-of-view, where does this leave us? It seems that, for some dogs, the neurons are still plastic enough, young enough, to change simply in the face of extinction or counterconditioning training: no medication is needed. In other cases, the positive techniques may “bend” the neurons enough to achieve a satisfactory outcome in the eyes of the owner. In still other cases, whether it’s in the face of initial difficulty or the rebound effect, medication is prescribed and success is a function of re-awakening the neuronal plasticity to achieve long-term success.

This research, as does all good research, leaves us with additional questions and predictions to be tested. Here are some that I am thinking about: counterconditioning for fear/anxiety issues should be more effective in younger dogs, while the neurons are still (naturally) plastic. Is this true? We don’t have any studies which address this. But these results might really get us thinking even more about trying to get to problems as soon as possible, when the dog is as young as possible.

Does counterconditioning, as opposed to the simpler extinction training used in this paper, truly further accelerate the process of readjusting the neurons? And of course, the basics: this occurs in mice… does it occur in dogs (most likely, yes!) but how about species or breed differences in levels of effect, or age of “crystallization” of fear responses? Perhaps you can think of additional questions or predictions: let us know, and I will respond with the best answers that we have!

Regardless of the answers to these questions, which we will have eventually, the research described here is important work. It will help us understand even further how the brain works, and therefore how we can help those in need, whether our own species or those species for which we are responsible.

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About drjimha

I am a professor of animal behavior at the University of Washington, specializing in social behavior with a focus on primates, killer whales, crows, and companion animals (dogs and cats). For fun, I love to fish saltwater (spinning, fly), snorkel, and travel with my wife Renee and son Andrew.

2 Responses to New Scientific Findings about How to Treat Fear in Dogs

Thanks for the report – this certainly gives ME more to chew on, since I’m in the process of gathering and collating what we really know of aggressive and frustration behaviors and what is really effective.

I’m sure they haven’t used fluoxetine specifically, but their own, and the research of others looked at in the last 20 years would lead me to be hopefully sceptical until proven fluoxetine with an exposure therapy (which one/s specifically?) much more efficient than what they’ve found.

One worry about using fluoxetine as far as I’m concerned is, the very well known and often pretty horrific side effects (http://www.drugs.com/fluoxetine.html) of both SSRI and SNRI drugs. I was on the SNRI Cymbalta and then Effexor for idiopathic neuropathic pain. While it did dampen the pain, it noticeably damped many cognitive abilities plus induced things like sudden and massive sleep attacks, general lethargy and tiredness as well as hampening abilities to take in and understand (sporadically, but still disturbing) environemtal situations – like what is that tree doing there and how about that sign to the right. Things just not quite making sense. Since dogs can’t tell us what they’re experiencing, we have no real way of assessing if their lack of aggressive behaviour is due to some new memories having replaced old ones or a simply “I can’t be bothered”.

There are other promising methods of changing the emotional content memories through a combination of chemicals and direct stimulation of the memories in the brain, once found, usually as I understand this, in the hippocampus, not the amygdala or the ventromedial prefrontal cortex (vmPFC). So … as you rightly ask – where dos this leave us?

Well, it gets us away from the hurtful claims of some trainers’ trainers, that “Return of Fear” only happens if you incompetently do a DS&CC (screen shot of this available upon request). It impresses upon us the fact, that exposure therapies can do wonders, when they work, but they are always tied to management strategies in which the unwanted behaviour does not get rehearsed, which puts us, if we can get the intervalic timing right, in the neighbourhood of memory reconsolidation (see Ledoux et al). And adding the second or third incident of less intensity to the mix occasionally (see Craske) can recall the original fear response memory at a lower intensity that doesn’t need to elicit the same unwanted behaviour, just spike the habituation curve and thus, according to her research reduce even further the probability and actual statistical occurrences of ROF.

But … until one can rule out the human side effects of fluoxetine in dogs, I have trouble getting overly excited about it.

greetings from Switzerland!

P.S. – with the help of google scholar I was able to drop both Effexor and Gaboentine in favor of r-Lipoic Acid, Acetyl-L-Carnitine, and good mixture of Omegs found in hemp oil (non THC type). All with solid peer reviewed research behind it. And, all those terrible side effects disappeared AND the pain/discomfort level is quite good.